Evidence map›Paper›PMID 39201392›Full record

ArticleInternational journal of molecular sciences2024

TNF Induces Laminin-332-Encoding Genes in Endothelial Cells and Laminin-332 Promotes an Atherogenic Endothelial Phenotype.

Assim Hayderi, Mulugeta Melkie Zegeye, Sare Meydan, Allan Sirsjö, Ashok Kumar Kumawat, Liza U Ljungberg

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Assim HayderiCardiovascular Research Centre, Department of Medical Sciences, School of Medicine, Örebro University, 70362 Örebro, Sweden.
Mulugeta Melkie ZegeyeCardiovascular Research Centre, Department of Medical Sciences, School of Medicine, Örebro University, 70362 Örebro, Sweden.ORCID 0000-0001-6952-8952
Sare MeydanCardiovascular Research Centre, Department of Medical Sciences, School of Medicine, Örebro University, 70362 Örebro, Sweden.
Allan SirsjöCardiovascular Research Centre, Department of Medical Sciences, School of Medicine, Örebro University, 70362 Örebro, Sweden.
Ashok Kumar KumawatCardiovascular Research Centre, Department of Medical Sciences, School of Medicine, Örebro University, 70362 Örebro, Sweden.ORCID 0000-0002-2244-9816
Liza U LjungbergCardiovascular Research Centre, Department of Medical Sciences, School of Medicine, Örebro University, 70362 Örebro, Sweden.ORCID 0000-0003-4253-3369

Funding

Foundation for Old Servants Dnr. 2020-01074 and 2021-01198
6 · The paper itself

Abstract

Laminins are essential components of the basement membranes, expressed in a tissue- and cell-specific manner under physiological conditions. During inflammatory circumstances, such as atherosclerosis, alterations in laminin composition within vessels have been observed. Our study aimed to assess the influence of tumor necrosis factor-alpha (TNF), a proinflammatory cytokine abundantly found in atherosclerotic lesions, on endothelial laminin gene expression and the effects of laminin-332 (LN332) on endothelial cells' behavior. We also evaluated the expression of LN332-encoding genes in human carotid atherosclerotic plaques. Our findings demonstrate that TNF induces upregulation of LAMB3 and LAMC2, which, along with LAMA3, encode the LN332 isoform. Endothelial cells cultured on recombinant LN332 exhibit decreased claudin-5 expression and display a loosely connected phenotype, with an elevated expression of chemokines and leukocyte adhesion molecules, enhancing their attractiveness and adhesion to leukocytes in vitro. Furthermore, LAMB3 and LAMC2 are upregulated in human carotid plaques and show a positive correlation with TNF expression. In summary, TNF stimulates the expression of LN332-encoding genes in human endothelial cells and LN332 promotes an endothelial phenotype characterized by compromised junctional integrity and increased leukocyte interaction. These findings highlight the importance of basement membrane proteins for endothelial integrity and the potential role of LN332 in atherosclerosis.

Indexed as

AtherosclerosisCell Adhesion MoleculesKalininLamininTumor Necrosis Factor-alphaCell AdhesionCells, CulturedEndothelial CellsGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsPhenotypePlaque, AtheroscleroticCell Adhesion MoleculesKalininLAMC2 protein, humanLamininlaminin alpha 3Tumor Necrosis Factor-alphaactivated endothelial cellsatherosclerosisECMlaminin-5monocytes migration

Identifiers

PMID39201392
PMCPMC11354388

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.